Introduction to Cardiovascular

Physiology
Sam Dudley, MD, PhD
Office: VA room 2A167
Tel: 404-329-4626
Email: sdudley@emory.edu
 Overview of the CV system
• Purposes
– Distribute metabolites and O2
– Collect wastes and CO2
– Thermoregulation
– Hormone distribution
• Components
– Heart – the driving force
– Arteries – distribution channels
– Veins - collection channels
– Capillaries – exchange points
Anatomy of the vasculature
Parallel and series design
• A given volume of blood
passes through a single
organ
• Blood entering an organ
RA LA has uniform composition
RV LV • Perfusion pressure is the
same for each organ
Organ 1 • Blood flow to each organ
Organ 2 can be controlled
independently
Organ 3
 Relationships among the vascular beds

• Flow is constant in each segment, so velocity and area are inversely related
• Pressure loss occurs mainly at the small arterioles, the resistance vessels
• The veins contain most of the blood
 Properties of arteries
• Elastic arteries • Muscular arteries
– Consists of the Aorta – Most of the named
and its large branches arteries
– Fairly distensible – Contain increased
because of high elastin
content smooth muscle
– Diastolic elastic recoil – Large lumen-to-wall
provides potential ratio
energy for flow when
the heart is not
contracting
Properties of the microcirculation
• Consists of arterioles, • Capillaries
capillaries, and – Exchange point
venules between blood and
• Arterioles interstitial fluid
– Reduced lumen-to-wall – Mechanisms of
ratio exchange include:
– Controlling point for • Diffusion
flow • Bulk flow
– Convert pulsatile to • Vesicular transport
steady flow
 Equations of exchange
• Diffusion is described by:
dc
Q = DA
dx
where Q is flow, A is area, D is the diffusion coefficient, and dc/dx is
the concentration gradient. D incorporates such constants as solubility,
temperature, and molecular size.
• Bulk flow is described by the Starling equation:

Q = k (∆P − ∆π )
where Q is the flow of water, ∆P is the hydrostatic pressure difference,
∆π is the osmotic pressure difference, and k is the hydrostatic
permitivity constant.
 Veins and lymphatics
• Veins
– Thin-walled, smaller amounts of smooth muscle or
elastin
– Slow flow, large cross-sectional area
– Acts a conduits and reservoirs
– Venoconstriction raises ventricular filling, cardiac
output
• Lymphatics
– Drains the interstitium
• Only route for of returning interstitial proteins
– Low flow (~2L/day)
 Cardiac anatomy

• The myocardial syncytium

– All atrial cells are coupled, all ventricular cells are coupled, the AV node
links the two
– Connections between cells are known as intercalated disks
• Electrical activation leads to contraction (EC coupling)
 Cardiac cellular anatomy
• Basic units is a sarcomere
(Z line to Z line)
– Think filaments of myosin
in the A band
– Thin filaments of actin in
the I band
• Sarcoplasmic reticulum
– Holds Ca2+
– Forms cisternae
– Approximation to T tubules
(sacrolemmal
invaginations) known as a
dyad
 Ca 2+ induced Ca 2+ release
Ca2+

K+ Na+ Ca2+
SARCOLEMMA

ATP ATP
Ca2+

SARCOPLASMIC
RyR2 Ca2+ Ca2+ RyR2 RETICULUM

ATP
Ca2+

SARCOMERE

• Ca2+ enters from sacrolemmal Ca2+ channels, diffuses to the SR Ca2+ release
channel (ryanodine receptor), and causes a large Ca2+ release.
• SR Ca2+ release raises intracellular Ca2+ from 10-7 M to 10-5 M, enough to
cause Ca2+ binding to troponin, displacing tropomyosin, causing actin-myosin
cross bridge cycling
The sliding filament hypothesis
Sliding filaments 2
Length-tension (Frank-Starling Effect)
• Length of a fiber
determines force
generation
• The major determinate
of length in the heart is
chamber volume
• The ascending limb
results from length-
dependent changes in
EC coupling
• The descending limb
derives mostly from the
number of thick and
thin filament cross
bridge interactions
 Pressure-volume loops
• Determinants of cardiac
output (stroke volume x
heart rate)
– Preload or ventricular end
diastolic volume
– Afterload or Aortic pressure
– Contractility or modulation
of active force generation
(ESPVR, inotropy)
– Ventricular compliance
(EDPVR, lusitropy)
ESV= end systolic volume;
– Heart rate EDV = end-diastolic volume;
SV = stroke volume
PV loop in heart failure
 Myocardial work
• Most myocardial work is potential work

W = ∫ PdV
• Myocardial O2 consumption is a function of myocardial
wall tension, contractility, and heart rate
• The law of Laplace:

T = Pr/ 2
where T is tension, P is pressure, and r is the radius.
– Larger ventricles have higher wall tension and O2 utilization to
produce the same pressure as smaller ones
The cardiac cycle
• Systole
– Phase 1: atrial contraction
– Phase 2: Isovolumetric
contraction
• Interval between
ventricular systole and
semilunar valve opening
– Phases 3 & 4: rapid and
reduced ejection (55-60%)
• Diastole
– Phase 5: Isovolumetric
relaxation
• Begins with closure of the
semilunar valves
– Phase 6: Rapid filling
• Opening of the AV valves
– Phase 7:Diastasis
 Hemodynamics

• Flow is a function of a pressure gradient and represents the conversion of

potential to kinetic energy
• Laminar flow is described by Poiseuille’s Law:
πr 4 ∆P
Q=
8ηl
Where ∆P is the pressure gradient, r is the radius, η is the viscosity, and l is the
length of the tube.
 Arterial pressure
• Rearranging Hook’s Law • Physiological determinants of
gives: ABP include:
– Heart rate
EdV
dP = • Raises V by decreasing
V runoff time
– Stroke volume
where E is the elastic
• ↑ SV ⇒ ↑ V, mean ABP,
constant (similar to dP, dV
Young’s modulus of – Increased peripheral vascular
elasticity), dP is the pulse resistance
pressure, dV is the net • Raises V by decreasing
runoff
systolic arterial uptake (∝
– Elastic constant generally
stroke volume), and V is increases with age
the mean arterial volume
 Venous return
• Low resistance, low • Factors affecting venous
return
pressure, high – Gravity
distensibility segment • Supine to erect transition
shifts ~ 500 mL of blood
• Contain 70-80% of to the leg veins, decreasing
cardiac output and ABP
circulating blood
– Valves – prevent retrograde
volume flow in dependent veins
– Muscle activity –
compresses veins to
enhance return
– Respiration – Negative
intrathoracic pressure
enhances venous return
 CV regulation

• Control of blood volume

– Neural
• Baroreceptors and
antidiuretic hormone
(ADH)
• Atrial tissue and
natriuretic peptides
– Endocrine
• ADH release in response
to increased osmolarity
• Renin-angiotensin-
aldosterone system
Control of blood volume
 Control of arterial pressure
• Baroreceptors
– Located in the carotid
sinus and aortic arch
– Receptor potential
varies with mean and
pulse pressures
– Efferent pathway is the
vagus (X) and
glossopharyngeal (IX)
nerves
Control of arterial pressure (cont)
• CNS centers
– Hypothalamus
– Medulla
• Autonomic
– Sympathetic
• Postganglionic adrenergic
fibers ⇒ vasoconstriction,
↑ chronotropy, ↑
lusitropy, and ↑ inotropy
• Postganglionic cholinergic
fibers ⇒ skeletal muscle
vasodilation
– Parasympathetic
• Largely opposes
sympathetic actions
Local control of flow
 Coupling the heart and vasculature
Cardiac function curve
Vascular function curve Normal
Pms − Pra equilibrium
CO =
R(1 + cv / ca )
Where Pms, Pra, R, cv,
and ca are the mean
systemic pressure,
right atria pressure,
total peripheral
resistance, arterial
and venous
capacitance,
respectively.
 References
1. Katz A.M., Physiology of the Heart,
Lippincott Williams & Wilkins, New
York, 2001.
2. Berne and Levy, Cardiovascular
Physiology, 7th Edition, Mosby, St. Louis,
1996.